[Objective]To evaluate the preemptive analgesic effect and safety with celecoxib in patients undergone the hip joint replacement.[Method]Fifty patients scheduled for elective hip joint replacement were randomly divided into two groups,celecoxib group and control group.Those of celecoxib group were given celecoxib 200 mg 24,12 h before incision.The operation was performed under extradural anesthesia by the same surgeons. All patients were given celecoxib 200 mg 8,24,36,48,60,72 h after the operation.Before celecoxib administration and after the operation,pain intensity was measured using visual analog scale(VAS),and analgesic requirements,side effects,hip joint ranges of motion,sleep states,hemorheology and phlebothrombosises messured with the ultrasonic wave were compared.[Result]There were no marked differences in the VAS pain scores before celecoxib administration between two groups.Compared with control group,the patients of celecoxib group had significantly lower VAS pain scores after the operation(P

Bis-(3′,5′) cyclic di-guanylate (c-di-GMP) is an almost ubiquitous intracellular second messenger in bacteria.Now it is known to regulate complex physiological processes, including mobility, adhesion, virulence and biofilm formation.The level of c-di-GMP is regulated by diguanylate cyclases (DGCs) containing GGDEF domains and phosphodiesterases (PDEs) containing EAL or HD-GYP domains.Recent studies have demonstrated that HD-GYP domain protein is a novel phosphodiesterase, which is also involved in the regulation of c-di-GMP degradation.This review highlights recent advances in the structure and biochemical functions of HD-GYP domain proteins, which might help to further clarify the mechanism of c-di-GMP signal system.

ObjectiveTo investigate the feasibility and superiority of video-assisted minithoracotomy surgery (VAMT) in treatment of adolescent patients with primary spontaneous pneumothorax. MethodsThe clinical data of 103 adolescent patients with spontaneous pneumothorax were analyzed retrospectively. VAMTS was performed in 56 cases and video-assisted thoracoseopic surgery(VATS) was performed in 47 cases. complications Statistical analysis were undergoing in middle-operation, post-operation and ambi-operation in the two groups were analyzed. ResultsNo statistically significant difference were found in blood loss ,operating time,pain grade, out-of-bed activity time, antibiotics use time,chest drainage time,hospital day pulmonary infection between the two groups( all P ＞0.05 ). The cost of hospitalization was lower in VAMTS group compare to VATS group ( P ＜ 0.05). ConclusionVAMT in treatment of adolescent patients with primary spontaneous pneumothorax had the advantage of simple performance, reliable effectiveness, practical,lower cost of hospitalization fee.

AIM:To investigate the effects of glucagon-like peptide-1 (GLP-1) receptor agonist exendin-4 on white adipose tissue (WAT) and the underlying mechanisms.METHODS:Male C57BL/6J mice (8 weeks) were chal-lenged by high-fat diet for 12 weeks, and were randomly divided into saline group and exendin-4 group.The mRNA expres-sion of sirtuin 1 (SIRT1), adipose triglyceride lipase (ATGL), TNF-αand adiponectin of WAT was detected by real-time PCR.3T3-L1 adipocytes or mouse embryonic fibroblasts cells were treated with exendin-4 for 24 h.The protein levels of SIRT1, ATGL and hormone-sensitive lipase (HSL) were determined by Western blot.RESULTS:Exendin-4 significantly decreased epididymal fat weight, fasting blood glucose and serum triglyceride levels ( P<0.05) , and reduced body weight and serum TNF-αlevel.The mRNA expression of SIRT1, ATGL and adiponectin in WAT was all significantly up-regulated by exendin-4, which were contrary to the down-regulation of TNF-αmRNA expression (P<0.05).Exendin-4 promoted the protein expression of SIRT1, ATGL, and HSL in 3T3-L1 adipocytes in a dose-dependent manner.Less lipid droplets with up-regulation of lipolytic protein expression were observed when combined with SIRT1 agonist treatment, which were suppressed by SIRT1 inhibitor.Deletion of SIRT1 led to larger adipocytes with more lipid droplets, and the effect of ex-endin-4 on the lipolysis disappeared when SIRT1 was deficient.CONCLUSION:Exendin-4 promotes lipolysis in WAT of obese mice via activation of SIRT1.

Objective To investigate the effects of morroniside on activation of caspase-3 in rats with focal cerebral ischemia/reperfusion. MethodsThe model was induced with occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. Vitamin E used for the positive control. The activity of caspase-3 was detected with spectrophotometry. ResultsCompared with sham group, the caspase-3 activity increased obviously in model rat. Compared with model group, Morroniside (30 mg/kg,90 mg/kg,270 mg/kg) decreased the activation of caspase-3 remarkably, which was dose-dependent (P<0.05). ConclusionMorroniside may reduce apoptosis by decreasing the activation of caspase-3 in rats.

ObjectiveTo investigate the effects of morroniside on IL-1β in rat cortex with focal cerebral ischemia/reperfusion.MethodsThe animal model was induced by occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. The content of IL-1β was detected with enzyme linked immunosorbent assay(ELISA).ResultsCompared with sham group, the content of IL-1β increased obviously in model rat. Compared with model group, morroniside(30 mg/kg, 90 mg/kg, 270 mg/kg) and colchicine (0.06 mg/kg) decreased the content of IL-1β significantly (P<0.001).ConclusionMorroniside may protect the cortex from inflammatory factor IL-1β.

Cerebral ischemia-reperfusion results in damage on neuron, leading to genes and proteins related to apoptosis activation. At the same time, generous cytokines released after cerebral ischemia-reperfusion can induce the apoptosis of the neuron. Many current studies have showed that the major damage mechanisms on apoptosis of the neuron are mitochondrion impairment, calcium overload, increased levels of oxygen radicals and so on. The advance research on the mechanism contributes to explore new neuroprotective drugs, and further identify the target and therapeutic effect of drug treatment.

ObjectiveTo investigate the effects of morroniside on super oxide dismutase (SOD) and neurons in rats cortex with focal cerebral ischemia/reperfusion. MethodsThe animal model was induced by middle cerebral artery occlusion with suture embolus, cerebral ischemia 30 min and reperfusion 3 d or 7 d. Vitamin E for the positive control. The content of SOD was detected with spectrophotometry and the nerve cells was observed with immunohistochemistry. ResultsCompared with model group, morroniside （270 mg/kg）increased the activity of SOD and the number of neurons （30 mg/kg, 90 mg/kg, 270 mg/kg） significantly. ConclusionMorroniside may have neuroprotective effect and increasing the activity of SOD in rats cortex.

Neural stem cells (NSCs), which will proliferate and differentiate into neurons and glial cells under certain conditions, involved in the repair of neurological function. This process is called neurogenesis. Focal cerebral ischemia-reperfusion injury is one of the most common diseases, which can induce the neurological functional deficits. It is significant to study the response and regulation of NSCs after focal cerebral ischemia-reperfusion injury. In this article, we reviewed the characteristics, molecular mechanisms, putative endogenous mediators and exogenous stimulators of neurogenesis in adult brain following ischemic injury, and response and regulation of drug in ischemic injury following neurogenesis.

Objective To investigate the effects of morroniside on total antioxidative capacity (T-AOC) in rat cortex with focal cerebral ischemia/reperfusion. Methods The animal model was induced with occlusion of middle cerebral artery. The T-AOC was detected with spectrophotometer. Results Compared with model group, morroniside （270 mg/kg） increased the T-AOC significantly. Conclusion Morroniside may take the neuroprotection through increased T-AOC of rat cortex.